Search

Thrombotic microangiopathy (TMA) is a frequent and severe complication in systemic lupus erythematosus (SLE). It is reported in almost 20-25% of renal biopsies of patients with lupus nephritis (LN) and is associated with a poor renal prognosis. We report the case of a patient suffering from an aggressive form of proliferative LN in association with thrombotic microangiopathy (TMA-LN), who was resistant to standard combined immunosuppressive treatment with corticosteroids and cyclophosphamide, as well as to plasma exchange (PEX). Eculizumab was given as a rescue therapy with an optimal clinical response. We performed a systematic review of the literature and identified 11 papers, published between 2011 and 2018, with a total of 20 patients, in which eculizumab was used, always as rescue therapy, to treat TMA-LN. All reported cases showed a positive clinical response to eculizumab with a high rate of remission. Even if sparse, available clinical cases and case series support the use of eculizumab in highly selected cases as rescue treatment for LN-TMA resistant to conventional combined immunosuppressive treatment., (Copyright by Società Italiana di Nefrologia SIN, Rome, Italy.)

Metabolic acidosis is frequently observed in clinical practice, especially among critically ill patients and/or in the course of renal failure. Complex mechanisms are involved, in most cases identifiable by medical history, pathophysiology-based diagnostic reasoning and measure of some key acid-base parameters that are easily available or calculable. On this basis the bedside differential diagnosis of metabolic acidosis should be started from the identification of the two main subtypes of metabolic acidosis: the high anion gap metabolic acidosis and the normal anion gap (or hyperchloremic) metabolic acidosis. Metabolic acidosis, especially in its acute forms with elevated anion gap such as is the case of lactic acidosis, diabetic and acute intoxications, may significantly affect metabolic body homeostasis and patients hemodynamic status, setting the stage for true medical emergencies. The therapeutic approach should be first aimed at early correction of concurrent clinical problems (e.g. fluids and hemodynamic optimization in case of shock, mechanical ventilation in case of concomitant respiratory failure, hemodialysis for acute intoxications etc.), in parallel to the formulation of a diagnosis. In case of severe acidosis, the administration of alkalizing agents should be carefully evaluated, taking into account the risk of side effects, as well as the potential need of renal replacement therapy.

Sepsis is a serious medical condition often complicated by multiorgan failure, especially in the intensive care unit setting. Acute renal failure is a frequent complication of sepsis, leading to increased hospital mortality risk and worsening of patient outcome. Despite recent advances in the treatment of sepsis and acute renal failure, the pathophysiological mechanisms of acute renal failure in sepsis is still not fully ascertained. The aim of this review is to illustrate the pathophysiological mechanisms that are involved in the development of acute renal failure in sepsis, with special regard to the systemic hemodynamic alterations, renal microvascular and inflammatory/immunological mechanisms.